In agreement, addition of IL-4 was able to increase FcγRIIb mRNA expression levels in the CML cell line KCL-22, and combined treatment with TKI could not antagonize elevated IL-4 expression, but even enhanced this effect (Supplementary Fig. S1), suggesting that TKI-persisting malignant upregulation could be mediated via altered cytokine levels in CML. This evidence concerns the gene FCGR2B and chronic myelogenous leukemia, BCR-ABL1 positive.